Secondary Logo

Journal Logo

Aortic Stenosis: Echocardiographic Diagnosis

von Homeyer, Peter MD, FASE*,†; Oxorn, Donald C. MD, CM, FRCPC, FACC*,‡

doi: 10.1213/ANE.0b013e31825c7d9b
Cardiovascular Anesthesiology: Echo Didactics
Free
SDC

Published ahead of print June 13, 2012 Supplemental Digital Content is available in the text.

From the *Department of Anesthesiology & Pain Medicine, Department of Surgery, and Division of Cardiology, University of Washington, Seattle, Washington.

The authors declare no conflicts of interest.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.anesthesia-analgesia.org).

Reprints will not be available from the authors.

Address correspondence to Peter von Homeyer, MD, FASE, Department of Anesthesiology & Pain Medicine, Box 356540, University of Washington, Seattle, WA 98195-6540. Physical street address for deliveries: 1959 N.E. Pacific St., Room BB1461, Seattle, WA 98195. Address e-mail to peter2@uw.edu.

Accepted April 16, 2012

Published ahead of print June 13, 2012

A 74-year-old man with coronary artery disease, hypertension, and hyperlipidemia is scheduled to undergo coronary artery bypass graft surgery. The intraoperative transesophageal echocardiogram (TEE) shows normal left ventricular function, moderate left ventricular hypertrophy, and an abnormal aortic valve (AV) with significant leaflet calcification (Video 1, see Supplemental Digital Content 1, http://links.lww.com/AA/A411).

The AV is part of the aortic root, which includes the AV annulus and leaflets, the sinuses of Valsalva, the sinotubular junction, and the proximal ascending aorta. The valve has 3 semilunar leaflets or cusps, the left, right, and the noncoronary cusps. There is no true AV annulus in the sense of an actual fibrous ring. Instead, the area of basal attachment of the AV leaflets, in the continuum of the left ventricular outflow tract (LVOT) and the ascending aorta wall, is usually referred to as the AV annulus.1

Back to Top | Article Outline

ECHOCARDIOGRAPHIC IMAGE ACQUISITION

Starting from a midesophageal (ME) 4-chamber view, the ME AV short-axis view is obtained by rotating the multiplane angle to 30 to 50 degrees. If necessary, slight advancement or withdrawal as well as turning the TEE probe to the patient's right is used to bring all 3 leaflets into view. A triangular opening can be visualized in systole, and a “Mercedes Benz” sign is seen when the valve is closed in diastole.

Rotation of the multiplane angle to 120 degrees to the ME AV long-axis view will image the LVOT and the aortic root. The AV leaflets seen on this view are the right coronary cusp anteriorly and most often the noncoronary cusp posteriorly. This view is frequently used to measure aortic root dimensions with measurements preferably performed in midsystole2 (Fig. 1).

Figure 1

Figure 1

Transgastric (TG) TEE views are necessary for the quantitative assessment of the AV. One can use either a deep TG long-axis view with the multiplane angle at 0 to 30 degrees or a TG long-axis view with the multiplane angle rotated to approximately 120 degrees (Fig. 2). Once properly aligned, 2 separate AV leaflets of equal length should be visible in any TG TEE view. Jets of mitral regurgitation (MR) can be misinterpreted as jets of aortic stenosis (AS) especially if anteriorly directed, as the Doppler beam frequently crosses the left atrium and the proximal ascending aorta. Color Doppler can help to identify concurrent MR, and pulsed-wave (PW) Doppler is useful to determine the time of onset of the interrogated jet with MR jets generally starting earlier in systole than jets of AS.

Figure 2

Figure 2

Back to Top | Article Outline

QUALITATIVE ASSESSMENT

A complete 2-dimensional (2D) examination of the AV assesses appearance, cusp number and mobility, leaflet coaptation, calcification, and size of the aortic root. The 3 most common causes of valvular stenosis are calcific AS, bicuspid AV, and rheumatic valve disease (Fig. 3).

Figure 3

Figure 3

Calcific AV disease is an active inflammatory disease, most often found in older patients3 (Video 1, see Supplemental Digital Content 1, http://links.lww.com/AA/A411). Calcifications typically involve the base of the leaflets without causing commissural fusion.4 The ME AV short-axis view shows the presence of calcification and what leaflets are involved. Assessment of leaflet mobility and separation are best done in the ME AV long-axis view sometimes with the help of M-mode echocardiography across the leaflet tips. Thin leaflets with a systolic separation of >15 mm excludes severe AS. Direct measurement of valve area by planimetry requires correct imaging angle and plane. The systolic orifice is frequently found at a higher plane than the Mercedes Benz sign visualized in diastole. Advancement and withdrawal of the TEE probe and color Doppler echocardiography is needed to find the narrowest orifice, and adjusting the 2D gain settings helps to identify the true margins of the orifice for planimetry.

Bicuspid AV is a congenital condition and patients often present as young adults with AS caused by superimposed calcifications.5 The echocardiographic picture includes 2 large cusps with 2 commissures and an elliptical valvular orifice (Video 2, see Supplemental Digital Content 2, http://links.lww.com/AA/A412). A raphe, usually located on the larger cusp can make the diastolic closed valve appear like a trileaflet valve. In bicuspid AV disease, identification of the narrowest orifice can be particularly challenging and measurements of the anatomical valve area by planimetry should be interpreted with caution. ME AV long-axis views can show “doming” of the leaflets into the ascending aorta. Patients with bicuspid AV should be evaluated for associated pathologies such as aortic aneurysm, coarctation, and patent ductus arteriosus.

Rheumatic valvular disease is an uncommon cause of AS in Europe and North America, although it is still very common in developing countries. The mitral valve is primarily involved with associated AV disease occurring in approximately 40% of the cases.6 Echocardiographic findings include commissural fusion and diffuse thickening of the leaflets, especially along the edges (Video 3, see Supplemental Digital Content 3, http://links.lww.com/AA/A413). Rheumatic valve thickening does not include acoustic shadowing as typically seen in calcific disease. The ME AV short-axis view often shows a triangular orifice. The morphology can be mistaken for calcific AS, hence the presence of similar changes to the mitral valve is an important part of the diagnosis.

Back to Top | Article Outline

QUANTITATIVE ASSESSMENT

TG TEE views are necessary for parallel alignment of the Doppler beam and the blood flow through the LVOT and AV. Misalignment is a common source of error in the quantification of AS. Careful search for the highest velocity jet is imperative, sometimes with the help of color Doppler, as this is the most parallel intercept angle. Continuous-wave (CW) Doppler flow is recorded for 3 beats, in case of an irregular heart rhythm for at least 5 beats.

The shape of the CW Doppler curve can give useful information about the severity and the localization of the obstruction. Jets of severe AS are high velocity, dense, and early peaking, whereas mild AS jets peak later in systole. Jets caused by dynamic LVOT obstruction have a classic dagger shape and peak very late in systole2 (Fig. 4). Fixed LVOT obstruction may look similar to valvular AS on CW Doppler recordings. The presence of a normal appearing AV on 2D TEE suggests subvalvular obstruction. Also, PW and color Doppler can help to determine the zone of flow acceleration and the level of obstruction.

Figure 4

Figure 4

The maximum pressure gradient (ΔPmax) across the AV is calculated using the simplified Bernoulli equation with VAV being the peak velocity:

However, when the proximal or LVOT velocity (VLVOT) exceeds 1.5 m/s, the modified Bernoulli equation should be used:

The mean pressure gradient is obtained by tracing the velocity envelope and integrated using the echocardiography system's software. A mean gradient above 40 to 50 mm Hg is consistent with severe AS (Table 1).

Calculated pressure gradients are dependent on flow through the valve and diagnostic error can occur in patients with altered volume flow rates. Examples for an increased volume flow rate are aortic regurgitation, anemia, pregnancy, and low systemic vascular resistance, where high-pressure gradients may be recorded, although the degree of stenosis is only mild. In contrast, patients with significant left ventricular systolic dysfunction, high systemic vascular resistance, or MR can have low gradients despite severe AS.

Flow convergence at the narrowest point of the stenosis causes conversion of potential to kinetic energy resulting in a reduction of pressure. After the narrowest point, there is some reconversion of kinetic into potential energy, a phenomenon called pressure recovery.7 CW Doppler measures velocities at the narrowest point of the jet, which can result in an overestimation of pressure gradients and a subsequent underestimation of calculated valve area, especially in the presence of a narrow aorta.

Assuming that stroke volumes (SV) in the LVOT and at the level of the stenotic AV (AS) are equal, the continuity equation is used to calculate AV area (AVA):

SV [cm3] is defined as the product of the cross-sectional area (CSA) [cm2] and the velocity-time integral (VTI) [cm]:

The CSA at the level of the AV is equal to the AVA. With the exception of the AVA, all variables can be measured using 2D (CSALVOT), PW Doppler (VTILVOT), and CW Doppler (VTIAS) echocardiography. To solve for the AVA, the equation is:

With TEE, the CSALVOT is best measured in the ME AV long-axis view just proximal to the AV in an inner-edge-to-inner-edge fashion. This is the anatomical level where the LVOT is most likely to be circular, whereas further upstream it is more elliptical. The LVOT diameter is measured and then used to calculate the CSALVOT using the formula:

Because of the squared relationship, measurement error has substantial consequences for the correct calculation of AVA. The AVA cutoff for severe AS is 1.0 cm2 (Table 1).

The VTILVOT is measured using PW Doppler. The sample volume is first placed into the jet next to the stenotic valve, which is often indicated by an audible valve-closing click. It is then moved apically and until a smooth velocity curve is seen indicating a position proximal to the flow acceleration zone. It is important to make CSA and VTI measurements at the same location in the LVOT.

Instead of measuring the velocities nonsimultaneously at the level of the valve and the LVOT, the double-envelope technique has been described and found to be equivalently accurate.8 Using the CW Doppler-derived flow curve, the VTI of both, the high-velocity outer envelope (VTIAS) and the more intense low-velocity inner envelope (VTILVOT), is traced and measured (Fig. 4). The dimensionless index (DI) or velocity ratio is a simplified parameter independent of cardiac output and LVOT diameter, which is a Doppler-only method and calculated using the formula:

A DI of ≤0.25 is consistent with severe AS (Table 1).

Table 1

Table 1

Table

Table

A way to simplify the continuity equation is to use peak velocities instead of VTI, which has the theoretical advantage of avoiding LVOT measurements and errors related to this.

Back to Top | Article Outline

DISCLOSURES

Name: Peter von Homeyer, MD, FASE.

Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.

Attestation: Peter von Homeyer approved the final manuscript.

Name: Donald C. Oxorn, MD, CM, FRCPC, FACC.

Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.

Attestation: Donald C. Oxorn approved the final manuscript.

This manuscript was handled by: Martin J. London, MD.

Back to Top | Article Outline

REFERENCES

1. Anderson RH. Clinical anatomy of the aortic root. Heart 2000; 84: 670–3
2. Baumgartner H, Hung J, Bermejo J, Chambers JB, Evangelista A, Griffin BP, Iung B, Otto CM, Pellikka PA, Quinones M. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr 2009; 22: 1–23
3. Otto CM. Calcific aortic valve disease: new concepts. Semin Thorac Cardiovasc Surg 2010; 22: 276–84
4. Adegunsoye A, Mundkur M, Nanda NC, Hage FG. Echocardiographic evaluation of calcific aortic stenosis in the older adult. Echocardiography 2011; 28: 117–29
5. Siu SC, Silversides CK. Bicuspid aortic valve disease. J Am Coll Cardiol 2010; 55: 2789–800
6. Marijon E, Celermajer DS, Tafflet M, El-Haou S, Jani DN, Ferreira B, Mocumbi AO, Paquet C, Sidi D, Jouven X. Rheumatic heart disease screening by echocardiography: the inadequacy of World Health Organization criteria for optimizing the diagnosis of subclinical disease. Circulation 2009; 120: 663–8
7. Bahlmann E, Cramariuc D, Gerdts E, Gohlke-Baerwolf C, Nienaber CA, Eriksen E, Wachtell K, Chambers J, Kuck KH, Ray S. Impact of pressure recovery on echocardiographic assessment of asymptomatic aortic stenosis: a SEAS substudy. JACC Cardiovasc Imaging 2010; 3: 555–62
8. Maslow AD, Mashikian J, Haering JM, Heindel S, Douglas P, Levine R. Transesophageal echocardiographic evaluation of native aortic valve area: utility of the double-envelope technique. J Cardiothorac Vasc Anesth 2001; 15: 293–9

Supplemental Digital Content

Back to Top | Article Outline
© 2012 International Anesthesia Research Society